Rodenticides are chemical agents designed to eliminate rodents, such as mice, by interfering with their normal biological processes. Unlike mechanical traps that cause physical trauma, these poisons are consumed and work internally, targeting physiological pathways required for survival. The method of death depends entirely on the active ingredient in the bait, with different chemical families causing distinct and often delayed mechanisms, ranging from disrupting blood clotting to causing neurological failure.
Disruption of Blood Clotting
The most common way poison kills mice involves anticoagulant rodenticides, which prevent the blood from clotting normally. These agents, including Warfarin, Brodifacoum, and Bromadiolone, interrupt the Vitamin K cycle in the liver. This cycle is responsible for recycling Vitamin \(\text{K}_{1}\) into its active form, which is necessary for synthesizing clotting factors (II, VII, IX, and X).
Anticoagulant compounds work by inhibiting the enzyme Vitamin K epoxide reductase. When this enzyme is blocked, the mouse cannot regenerate active Vitamin \(\text{K}_{1}\), and the liver stops producing functional clotting factors. Since existing clotting factors have a short half-life, their concentration rapidly drops within a few days. The mouse’s blood loses its ability to coagulate, causing continuous bleeding from even small internal injuries.
Death occurs due to widespread internal hemorrhage that leads to hypovolemic shock and circulatory failure. First-generation anticoagulants like Warfarin require multiple feedings to reach a lethal dose, while second-generation compounds are potent enough to cause death after a single feeding. Clinical signs, such as weakness and pale gums, are delayed, often appearing three to seven days after ingestion, once existing clotting factors are depleted.
Neurological Failure and Edema
A different group of rodenticides, exemplified by the neurotoxin Bromethalin, attacks the central nervous system. Once ingested, Bromethalin is metabolized in the liver into desmethylbromethalin, its active form. This metabolite is highly lipid-soluble, allowing it to easily cross the blood-brain barrier.
Inside the central nervous system, desmethylbromethalin limits the production of adenosine triphosphate (ATP), the cell’s energy currency, by uncoupling mitochondrial oxidative phosphorylation. The resulting lack of ATP causes the failure of the \(\text{Na}/\text{K}\) ATPase pump, disrupting the sodium-potassium gradient across nerve cell membranes. This ionic imbalance leads to an influx of sodium and water into the nerve cells, causing massive fluid buildup known as cerebral edema.
The swelling increases pressure inside the skull, compressing and damaging nerve cell axons. This elevated intracranial pressure results in neurological symptoms, including tremors, seizures, and eventual paralysis. Death is often caused by respiratory depression or arrest, as the pressure on the brain stem interferes with the neural control of breathing.
Calcium Overload and Organ Damage
Another mechanism involves rodenticides containing Cholecalciferol, which is a massive overdose of Vitamin \(\text{D}_{3}\). While small amounts of Vitamin \(\text{D}_{3}\) are necessary for health, toxic doses disrupt the body’s calcium and phosphorus balance. The excess Cholecalciferol is converted into metabolites that cause a rapid, uncontrolled increase in calcium absorption from the intestines and mobilization from the bones.
This results in hypercalcemia, an excessive concentration of calcium in the blood. The high calcium and phosphorus levels lead to the metastatic mineralization of soft tissues, causing calcium deposits to form where they should not. The organs most frequently affected are the kidneys, heart, and blood vessels.
The calcification of the kidneys leads to acute renal failure, which is the most common cause of death. Clinical signs, such as increased thirst and urination, can begin within 12 to 48 hours, but fatal organ failure typically occurs between three and seven days after ingestion.
Toxicity, Timeline, and Accidental Exposure Treatment
The speed at which a mouse is killed varies based on the chemical used and the dosage consumed. Anticoagulant rodenticides are the slowest-acting, delaying death by three to seven days because existing clotting factors must be depleted first. In contrast, the neurotoxin Bromethalin acts quickly, causing severe signs and often death within hours to 36 hours. Cholecalciferol falls in the middle, with clinical signs appearing within a day, but fatal organ damage developing over three to seven days.
Accidental ingestion by pets or humans requires immediate action, as treatment is dictated by the poison type. For anticoagulant rodenticides, the established medical intervention is the administration of Vitamin \(\text{K}_{1}\) to restore the body’s ability to synthesize clotting factors. Depending on the specific anticoagulant, this treatment may need to continue for several weeks to months.
For both Bromethalin and Cholecalciferol, there is no specific antidote available. Treatment for these non-anticoagulant poisonings is largely supportive, focusing on aggressive decontamination, such as inducing vomiting or using activated charcoal, and managing symptoms. Cholecalciferol exposure requires long-term management to lower high calcium levels using specialized medications and intravenous fluids to prevent permanent organ damage.